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Archives of cardiovascular diseases
Volume 105, n° 8-9
pages 461-462 (août 2012)
Doi : 10.1016/j.acvd.2011.05.014
Received : 9 July 2010 ;  accepted : 26 May 2011
Coronary microvasculopathy and intracardiac thrombosis in antiphospholipid syndrome
Coronaropathie microvasculaire et thrombose intracardiaque dans le syndrome des antiphospholipides

Razvan Onea a, , Philippe Germain b, André Zimmermann c
a Laboratoire des explorations fonctionnelles, Hôpital Civil de Colmar, 39, avenue de la Liberté, 68024 Colmar, France 
b Nouvel Hôpital Civil, 67000 Strasbourg, France 
c Hôpital Albert-Schweitzer, 68003 Colmar, France 

Corresponding author.

Keywords : Antiphospholipid syndrome, Intracardiac thrombosis, Cardiac microvasculopathy

Mots clés : Syndrome des antiphospholipides, Thrombose intracardiaque, Microvasculopathie cardiaque

Abbreviations : APS, CMR, LV

A 57-year-old woman, with a history of recurrent deep venous thromboses, was admitted for progressive dyspnoea rapidly improved by diuretic treatment; her electrocardiogram showed deeply inverted T-waves in precordial leads. Pulmonary embolism was dismissed by a normal lung scan. Early coronary angiography was completely normal. However, echocardiography revealed a bilobulated mass attached to the apex of an apparently normally contracting LV, compatible with mural thrombus (Figure 1A; Appendix A), prompting heparin therapy.

Figure 1

Figure 1. 

A. Transthoracic echocardiography shows a bi-lobulated mass attached to the apex of the left ventricle. B. Cardiovascular magnetic resonance: inversion recovery delayed-enhanced four-chamber left ventricle view acquisition with phase-sensitive detection demonstrates the resolution of the intracardiac mass after anticoagulation and subendocardial delayed enhancement pattern of ischaemia in the related left ventricle apex.


CMR examination performed 2 weeks later demonstrated a small apical area of subendocardial delayed contrast enhancement, characteristic of ischaemic injury, with resolution of the previously described mass (Figure 1B) and no obvious LV wall motion abnormalities (Appendix A).

Laboratory tests were remarkable for positive immunoglobulin G and M anticardiolipin antibodies. Primary APS was diagnosed as no other underlying disease could be identified, the anticardiolipin antibodies remaining elevated 13 weeks later.

Our findings suggest that myocardial ischaemia in this patient was caused by thrombotic cardiac microvasculopathy. Eventually, the ischaemically injured overlying endocardium would act as a trigger for clot formation. However, mural thrombosis into a normally contracting LV remains most unusual. We therefore believe that systemic APS-related coagulopathy played a substantial role in both events.

This case points toward a possible pathogenic mechanism for intracardiac thrombosis in APS, illustrating the subtle interplay of microvascular and intracardiac thrombotic phenomena in this setting. It also emphasises the prominent role of CMR imaging in the diagnostic work-up of these difficult cases.

Disclosure of interest

The authors declare that they have no conflicts of interest concerning this article.

Appendix A. Supplementary data

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 Video 1 
Video 1. 

Four-chamber view transthoracic echocardiography performed on presentation revealed a mobile mass attached to the apex of a normally contracting left ventricle.

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 Video 2 
Video 2. 

Four-chamber steady-state free precession cine-imaging performed at 2 weeks follow-up demonstrated no obvious left ventricular locoregional contraction anomalies (to consider in conjunction with Video 3).

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 Video 3 
Video 3. 

Two-chamber steady-state free precession cine-imaging performed at 2 weeks follow-up demonstrated no obvious left ventricular locoregional contraction anomalies (to consider in conjunction with Video 2).

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